Abstract

This study was undertaken to elucidate the short-term effect of iron on the hyperplastic lesions of experimental hepatocarcinogenesis. The Solt-Farber's resistant hepatocyte model was chosen for the experiment, and Sprague-Dawley rats wee divided into six groups: normal control, iron-rich diet administration with or without hydroxyquinoline. The iron content, microscopic changes, bromodeoxyuridine(BrdU) labelling index and the DNA polidy were studied. In the carcinogen administered group, oval cell proliferation and consecutive hyperplastic lesions of hepatocyte developed regardless of iron administration. The hepatic iron content was increased rimarkably by iron administration, but gradually decreased as the hyperplastic lesions developed in carcinogen administered groups. Although the administration of iron without carcinogen induced hepatic accumulation of stainable iron, the hyperplastic lesions appeared to be lack of it. BrdU labelling indices of the oval cells and the hyperplastic lesions of hepatocyte were very high and were not significantly altered by iron administration. Most liver cells had diploid or tetraploid DNA content, but there was an increase of diploidy as the development of hyperplastic lesions regardless of iron administration. The results indicate that the chemical carcinogen-induced hyperplastic lesions of hepatocyte do not accumulate iron, and that short-term iron administration does not affect the development of hyperplastic lesions and their proliferative activity and DNA ploidy.

• Keywords: Hepatic carcinogenesis;Hyperplastic lesions;Iron;DNA ploidy;Bromodexyuridine